Thoracic Outlet Syndrome in Sport: A Systematic Review.

Thoracic outlet syndrome (TOS) is a rare and heterogeneous syndrome secondary to a compression of the neurovascular bundle in the thoracic outlet area. Muscle hypertrophy is recognized to induce vascular or neurogenic compression, especially in sports involving upper-arm solicitation. Athletes represent a distinctive population because of a specific management due to an ambitious objective, which is returning to high-level competition. We evaluated the scientific literature available for the management of TOS in athletes. Article research extended to March 2021 without other restriction concerning the date of articles publication. The search was performed independently by two assessors. A first preselection based on the article titles was produced, regarding their availability in English or French and a second preselection was produced after reading the abstracts. In case of doubt, a third assessor's advice was asked. Case reports were selected only if the sport involved was documented, as well as the level of practice. Cohorts were included if data about the number and the sport level of athletes were detailed. Seventy-eight articles were selected including 40 case reports, 10 clinical studies and 28 reviews of literature. Baseball pitchers seem to be highly at risk of developing a TOS. The surgical management appears particularly frequent in this specific population. The prognosis of TOS in athletes seems to be better than in the general population, possibly due to their better physical condition and their younger age. Some studies showed interesting and encouraging results concerning return to previous sport level. Literature shows a strong link between TOS and certain sports. Unfortunately, this syndrome still lacks rigorous diagnostic criteria and management guidelines for athletes.

Rotator Cuff Tenocytes Differentiate into Hypertrophic Chondrocyte-Like Cells to Produce Calcium Deposits in an Alkaline Phosphatase-Dependent Manner.

Calcific tendonitis is a frequent cause of chronic shoulder pain. Its cause is currently poorly known. The objectives of this study were to better characterize the cells and mechanisms involved in depositing apatite crystals in human tendons. Histologic sections of cadaveric calcified tendons were analyzed, and human calcific deposits from patients undergoing lavage of their calcification were obtained to perform infrared spectroscopy and mass spectrometry-based proteomic characterizations. In vitro, the mineralization ability of human rotator cuff cells from osteoarthritis donors was assessed by alizarin red or Von Kossa staining. Calcifications were amorphous areas surrounded by a fibrocartilaginous metaplasia containing hypertrophic chondrocyte-like cells that expressed tissue non-specific alkaline phosphatase (TNAP) and ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), which are two key enzymes of the mineralization process. Calcific deposits were composed of apatite crystals associated with proteins involved in bone and cartilage development and endochondral bone growth. In vitro, tenocyte-like cells extracted from the rotator cuff were able to mineralize in osteogenic cultures, and expressed TNAP, type X COLLAGEN, and MMP13, which are hypertrophic chondrocytes markers. The use of a TNAP inhibitor significantly prevented mineral deposits. We provide evidence that tenocytes have a propensity to differentiate into hypertrophic chondrocyte-like cells to produce TNAP-dependent calcium deposits. We believe that these results may pave the way to identifying regulating factors that might represent valuable targets in calcific tendonitis.

Jumper's knee mechanical consequences in professional basketball players: the "Camel's Back curve".

PURPOSE: Jumper's knee is characterized by an anterior knee pain during tendon palpation and can be classified in overuse pathologies, secondary to repetitive jumps. The prevalence is high in professional basketball players. It is responsible for an alteration of the motor control inducing a strength deficit of the quadriceps. We aimed to describe an isokinetic curve anomaly, a double-humped curve called "Camel's Back curve", consequence of a jumper's knee history. METHODS: 170 Professional basketball players were enrolled (24.8 ± 4.6 years; 91.8 ± 12.0 kg, 194 ± 9.0 cm). All players performed isokinetic tests of the knee extensors on a concentric mode at the angular speed of 60°/s and 180°/s. RESULTS: 43 players had a jumper's knee history and 35 (81%) had a "Camel's Back curve" at 60°/s. The sensitivity and the specificity of this curve were 81.3% and 100%, respectively. The minimum torque of strength was decreased from 12 to 18% compared to the 2 maximal peaks. Yet, the strength measured every 5° of ROM was significantly different between the players with "Camel's Back curve" and those with normal curve. CONCLUSIONS: "Camel's Back curve" had never been described in that context. It may be secondary to a protective inhibitory mechanism which could alter jumping. The presence of a "Camel's Back curve" would enable clinicians to adapt physical preparation, knee rehabilitation, and trainings to improve players performances.

IMSYC immunologic synovitis score: A new score for synovial membrane characterization in inflammatory and non-inflammatory arthritis.

OBJECTIVES: Krenn synovitis Score has been developed by Krenn et al. in order to assess synovitis severity and is used in synovial research. Cell signature of synovial tissue can be studied using immunohistochemistry and is of interest as a biomarker for both prognosis and prediction of response to treatment. However, no synovitis score including immunohistochemistry exists yet. In order to answer this unmet need, we propose a new Immunologic Synovitis score (IMSYC) adding 5 components to the Krenn score: CD68, CD3, CD20, CD31 and Ki67 immunostaining. In this study, we aimed to validate this new IMSYC by studying its diagnostic performances in a well-defined collection of synovial samples. METHODS: Synovial samples from patients were obtained during surgical procedures. CD68, CD3, CD20, CD31 and KI67 immunohistochemistry were performed. RESULTS: In total, 77 patients were included. In total, 45 were females, mean age was 63.1 years. Forty had inflammatory arthritis, mainly rheumatoid arthritis (31/40). Non inflammatory arthritis group included 35 patients with mainly osteoarthritis. Mean Krenn score and IMSYC were significantly higher in the inflammatory group (P<0.001). ROC analysis of diagnostic performances determined the score of 13.5 out of 24 as the cut-off that gave the best ratio for discrimination between inflammatory and non-inflammatory arthritis with a sensitivity of 71.8% and specificity of 98%. CONCLUSION: We propose a new synovitis score including immunohistochemistry. This score has a better sensitivity and specificity than the Krenn score and represents a more functional synovitis evaluation. IMSYC could be further used in better categorizing synovial tissue phenotype and give a basis for tissue driven therapy.

The enigmatic role of IL-38 in inflammatory diseases.

IL-38 is the most recently discovered cytokine of the IL-1 family and is considered a potential inhibitor of the IL-1 and Toll-like receptor families. IL-38 exerts anti-inflammatory properties, especially on macrophages, by inhibiting secretion of pro-inflammatory cytokines, leading to reduced T-lymphocyte TH17 maturation. IL-38 has been studied most extensively in the context of chronic inflammatory diseases, particularly arthritis, where it is considered an attractive new drug candidate. IL-38 research has entered a new phase, with the realization that IL-38 is important in the pathophysiology of TH17 dependent-diseases (psoriasis, psoriatic arthritis and ankylosing spondylitis). In this review, we provide a critical evaluation of several controversial issues concerning IL-38 function and regulation. There is effectively contrasting data regarding IL-38: it is produced in conditions such as apoptosis, necrosis or inflammation, but data is lacking regarding IL-38 processing and biological function. Furthermore, the receptor for IL-38 has yet to be identified, although three candidate receptors - IL-1R1, IL-36R and IL-1RAPL1-have been proposed. Future studies will hopefully uncover new aspects of this enigmatic cytokine.

Involvement of sphingosine kinase/sphingosine 1-phosphate metabolic pathway in spondyloarthritis.

Spondyloarthritis (SpA) is a relatively common chronic inflammatory joint disorder, with a prevalence of about 0.2-0.5% worldwide. The primary target of the pathological process is the enthesis, where tendons and ligaments attach to underlying bone. These insertion sites are hotspots of bone formation (enthesophytes), which can lead to ankylosis. Unfortunately, the mechanisms causing the onset and progression of entheseal ossification remain largely unknown. Sphingosine 1-phosphate (S1P), a lipid generated after sphingosine phosphorylation by sphingosine kinases 1 and 2 (SK1/2), plays important roles in cell proliferation, differentiation and survival. S1P regulates fundamental biological processes such as cell cycle, inflammatory response or bone homeostasis. Indeed, S1P has been involved in some of most-spread skeletal diseases such as rheumatoid arthritis or osteoarthritis. On the other hand, the implication of S1P in SpA has not been explored yet. In the present work, we observed by ELISA that S1P content was significantly increased in the serum of SpA patients (6.1±4.2µM, n=21) compared to healthy donors (1.6±0.9µM, n=12). In vitro, gene expression of SK1 and SK2 as well as their activity were increased during differentiation of primary murine chondrocytes and osteoblasts into mineralizing cells. In addition, mRNA of the S1P-specific transporter Spns2 and S1P secretion were augmented. Using the pharmacological drugs SKi (SK pan-inhibitor), PF-543 (SK1 specific inhibitor) or K-145 (SK2 specific inhibitor), we showed that the inhibition of SK1 and/or SK2 decreased matrix mineralization, alkaline phosphatase activity and the mRNA expression of Runx2 and Bglap in chondrocytes and osteoblasts. To our knowledge, this is the first study indicating that S1P levels are significantly increased in serum from SpA patients. Moreover, we showed in vitro that SK activity was involved in the mineralization capacity of osteoblasts and chondrocytes. S1P metabolic pathway may represent an ingenious therapeutic target for SpA in the future.